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Cell Metab. 2017 Jul 5;26(1):198-211.e5. doi: 10.1016/j.cmet.2017.06.015.

The Sense of Smell Impacts Metabolic Health and Obesity.

Author information

1
Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA; The Paul F. Glenn Center for Aging Research, University of California, Berkeley, Berkeley, CA, USA; Diabetes and Obesity Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA, USA.
2
Department of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Gleueler Strasse 50, Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, Cologne, Germany; Max Planck Institute for Biology of Ageing, Cologne, Germany and Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) Cologne, Germany; Department of Genetics and Complex Diseases and Sabri Ülker Center, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
3
Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA; The Paul F. Glenn Center for Aging Research, University of California, Berkeley, Berkeley, CA, USA.
4
The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA, USA.
5
Max Planck Institute for Biology of Ageing, Cologne, Germany and Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) Cologne, Germany.
6
Department of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Gleueler Strasse 50, Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, Cologne, Germany.
7
Nutritional Sciences and Toxicology, University of California, Berkeley, Berkeley, CA, USA.
8
Department of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Gleueler Strasse 50, Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, Cologne, Germany; Max Planck Institute for Biology of Ageing, Cologne, Germany and Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) Cologne, Germany. Electronic address: bruening@sf.mpg.de.
9
Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA; The Paul F. Glenn Center for Aging Research, University of California, Berkeley, Berkeley, CA, USA. Electronic address: dillin@berkeley.edu.

Abstract

Olfactory inputs help coordinate food appreciation and selection, but their role in systemic physiology and energy balance is poorly understood. Here we demonstrate that mice upon conditional ablation of mature olfactory sensory neurons (OSNs) are resistant to diet-induced obesity accompanied by increased thermogenesis in brown and inguinal fat depots. Acute loss of smell perception after obesity onset not only abrogated further weight gain but also improved fat mass and insulin resistance. Reduced olfactory input stimulates sympathetic nerve activity, resulting in activation of β-adrenergic receptors on white and brown adipocytes to promote lipolysis. Conversely, conditional ablation of the IGF1 receptor in OSNs enhances olfactory performance in mice and leads to increased adiposity and insulin resistance. These findings unravel a new bidirectional function for the olfactory system in controlling energy homeostasis in response to sensory and hormonal signals.

KEYWORDS:

diet-induced obesity; energy balance; hyperosmia; hyposmia; insulin resistance; insulin-like growth factor 1 receptor; lipolysis; olfactory sensory neuron; thermogenesis

PMID:
28683287
DOI:
10.1016/j.cmet.2017.06.015
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